Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using a highly sensitive radioimmunoassay, elevated plasma immunoreactive endothelin (ir-ET) levels were found in patients with diabetes mellitus (1.88 +/- 0.12 pmol/L, mean +/- SEM, n = 100), patients undergoing maintenance hemodialysis (4.28 +/- 0.76 pmol/L, n = 14), patients with acute myocardial infarction (3.43 +/- 1.03 pmol/L, n = 6), and patients with subarachnoid hemorrhage (4.92 +/- 0.64 pmol/L, n = 14) (normal controls: 0.54 +/- 0.05 pmol/L, n = 19). ir-ET was also present in urine (2.1 +/- 0.3 pmol/L, n = 12), breast milk (6.8 +/- 1.6 pmol/L, n = 16), and saliva (2.0 +/- 0.2 pmol/L, n = 15) obtained from healthy subjects. Chromatography studies verify the identity of endothelin. Fast protein liquid chromatography (FPLC) showed one peak in the normal plasma extract, three peaks in the plasma extracts from diabetic patients and patients undergoing maintenance hemodialysis, three peaks in the urine extract, four peaks in the milk extract, and five peaks in the saliva extract. When the materials eluting in the void volume on FPLC of urine and saliva extracts were loaded onto a Sephadex G-25 column, the ir-ET was eluted in a higher molecular weight region. Incubation of endothelin-1, endothelin-2, and endothelin-3 in urine for 5 h showed that the total amount of ir-ET decreased to less than 30% of the initial levels, suggesting that endothelins are very unstable in urine.
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PMID:Immunoreactive endothelin in human plasma, urine, milk, and saliva. 172 88

Proliferation in the intimal layer and medial necrosis are the most consistent findings in the cerebral artery following subarachnoid haemorrhage (SAH) in man. Recently, SEM studies from our laboratory have also shown marked endothelial injury as demonstrated by a profuse platelet carpet. Myofibroblasts proliferate in response to the platelet derived growth factor (PDGF), and abundant collagen is present in the vessel wall. We have employed experiments using fibroblast-populated collagen lattices to study cerebrospinal fluid (CSF) from patients with recent SAH. Isolated rat tail collagen and cultured human dermal fibroblasts are mixed together, placed in 35 mm Petri dishes, and allowed to gel. CSF samples are placed on the surface of the collagen lattice, using 0.2 ml saline for control. The collagen lattices are then incubated and daily measurements recorded. We found that CSF samples from patients with recently ruptured aneurysms significantly accelerate contraction of the collagen lattice. The factor in CSF is heat stable and has a molecular weight of less than 6000.
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PMID:Cerebrospinal fluid factors following subarachnoid haemorrhage accelerate collagen lattice contraction by fibroblasts. 197 Jun 25

The purpose of this study was to evaluate the constrictive effect of endothelin, a peptide vasoconstrictor derived from endothelium, on canine basilar artery. Constriction was measured by an isometric tension recording method. Endothelin induced prolonged contraction of canine basilar artery in a dose-dependent fashion, the estimated concentration at 50% contraction being (2.1 +/- 0.5) X 10(-9) M (mean +/- SEM). Removal of endothelium significantly augmented the arterial response to endothelin. In Ca(++)-free medium no contractile response was elicited at 10(-8) M endothelin. Papaverine (10(-4) M) and nicardipine (10(-8) M), a calcium channel blocker, almost completely inhibited the contraction induced by 10(-8) M endothelin. Pretreatment with nicardipine (10(-8) - 10(-6) M) also significantly suppressed the response to endothelin. Acetylcholine (10(-7) - 10(-4) M), adenosine triphosphate (10(-7) - 10(-5) M), and thrombin (0.1 and 1.0 U/ml) dose-dependently inhibited contraction of canine basilar artery in response to 3 X 10(-9) M endothelin. These results show that endothelin has a potent constrictive effect on canine basilar artery and suggest that this substance may play an important role in the pathogenesis of vasospasm following subarachnoid hemorrhage.
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PMID:Pharmacological effect of endothelin, an endothelium-derived vasoconstrictive peptide, on canine basilar arteries. 248 63

Hyponatremia is common following aneurysmal subarachnoid hemorrhage and has been linked to the syndrome of inappropriate secretion of antidiuretic hormone. However, the demonstration of volume depletion and natriuresis in some patients has suggested that salt wasting is a more likely etiology. Atrial natriuretic factor appears to play a role in both central and peripheral regulation of sodium homeostasis. To investigate the behavior of circulating atrial natriuretic factor following subarachnoid hemorrhage, we studied 25 patients with intracranial aneurysms: 21 after acute subarachnoid hemorrhage and four without evidence of recent rupture. Atrial natriuretic factor was measured by radioimmunoassay of extracted plasma (normal value, 20.8 +/- 24.6, mean +/- 3 SD). Mean +/- SEM plasma atrial natriuretic factor concentration was elevated to 84 +/- 25 pg/ml on Day 1, rose to 134 +/- 29 pg/ml on Day 3, and fell to 86 +/- 17 pg/ml by Day 7 after subarachnoid hemorrhage (p less than 0.01). In two patients (9.5%) who developed hyponatremia after aneurysm rupture, plasma concentrations were no different from that in the group as a whole; concentrations in patients with no evidence of recent subarachnoid hemorrhage were not elevated. Neither fluid administration nor timing of surgery could account for the elevated concentrations. We conclude that concentrations of circulating atrial natriuretic factor are elevated after subarachnoid hemorrhage but do not solely account for the accompanying hyponatremia.
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PMID:Plasma atrial natriuretic factor and subarachnoid hemorrhage. 297 Jul 2

Arachidonic acid (AA) metabolites may play an important role in the pathogenesis of cerebral vasospasm which complicate subarachnoid hemorrhage. Authors have studied levels of 4 major AA metabolites in lumbar CSF samples and in CSF collected from perianeurismatic cisterns of 40 patients admitted with diagnosis of subarachnoid hemorrhage. Lumbar levels of AA metabolites are significantly higher in SAH patients than in control cases; moreover, cisternal CSF levels of PGD2, TxB2 and LTC4 are significantly higher than lumbar levels. Cisternal CSF levels (expressed in pg/ml +/- SEM) are in the "spasm" group: PGD2: 1129.62 +/- 146.33; 6-keto-PGF1 alpha: 214.2 +/- 19.96; TxB2: 4350.25 +/- 656.87; LTC4: 2582.19 +/- 381.83. In the "no spasm" group: PGD2 460.1 +/- 55.89; 6-keto-PGF1 alpha: 306.37 +/- 88.74; TxB2: 5752.5 +/- 899.25; LTC4: 812.92 +/- 142.06. Statistical analysis (paired t-test) shows values significantly higher for cisternal levels of PGD2 (P less than 0.005) and LTC4 (P less than 0.005) in patients presenting vasospasm. This suggests the importance of the subarachnoidal clot as a source of vasoactive compounds. Higher levels of leukotriene C4 in patients presenting vasospasm suggest a role for the compound in the genesis of local inflammatory processes and morphological changes of the arterial wall.
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PMID:A study on cisternal CSF levels of arachidonic acid metabolites after aneurysmal subarachnoid hemorrhage. 313 38

The effect of subarachnoid hemorrhage on metabolic rates in rabbit cerebral arteries was investigated by measuring adenosine triphosphate (ATP) content and L-lactate release. The mean +/- SEM ATP content was 0.38 +/- 0.02 mumol/g wet wt in control rabbit basilar arteries (n = 6). The ATP content decreased significantly to 0.17 +/- 0.02 mumol/g wet wt 2 days after experimental subarachnoid hemorrhage (n = 6), although only a slight decrease was detected in the basilar arteries 2 days after cisternal injection of the same amount of artificial cerebrospinal fluid. Hypoxia significantly decreased ATP content in the control basilar arteries to 0.26 +/- 0.04 mumol/g wet wt (n = 6). The same degree of hypoxia did not decrease ATP content in the basilar arteries after subarachnoid hemorrhage. Release of L-lactate was significantly higher from the arteries after subarachnoid hemorrhage than from the control arteries under both aerobic and hypoxic conditions. Our results indicate that subarachnoid hemorrhage induced an alteration of metabolic rates in rabbit cerebral arteries. The oxygen-requiring pathways to synthesize ATP may be important in control cerebral arteries; however, after experimental subarachnoid hemorrhage, the main pathway in the cerebral arteries may shift from oxygen-requiring pathways to an anaerobic glycolytic pathway.
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PMID:Metabolic alterations in rabbit cerebral arteries caused by subarachnoid hemorrhage. 338 59

Release of arachidonate metabolites from isolated canine cerebral arteries into perfusing medium were estimated using radioimmunoassay (RIA) in vitro. The cerebral arteries were isolated from dogs sustained experimental subarachnoid hemorrhages (SAH) and the results were compared with that of normal canine cerebral arteries. The amount of 6-Keto-PG F1 alpha (stable metabolite of PGI2) and PGE2 released from normal cerebral arteries were 455 +/- 84 (n = 7) and 177 +/- 72 (n = 8) ng/min/g dry weight (mean +/- SEM), respectively. Among other arachidonate metabolites, TXB2 (stable metabolite of TXA2), PGF2 alpha, PGD2 were also measured, but release of these arachidonate metabolites were little compared with PGI2 or PGE2. The amount of 6-Keto-PGF1 alpha and PGE2 released from the cerebral arteries subjected to subarachnoid hemorrhage were 110 +/- 34 (n = 6), 169 +/- 40 (n = 6) ng/min/g dry weight respectively. In SAH group, release of 6-Keto-PGF1 alpha had diminished remarkably, but no remarkable quantitative change were seen among other arachidonate metabolite between normal and SAH groups. The diminution of PGI2 release in the cerebral artery subjected to SAH may be involved in the pathogenesis of cerebral vasospasm. The release of PGs from canine pial arteries induced by the exposure of the pial arteries to red blood cell hemolysate was also estimated by RIA. The release of PGE2 tended to increase following to exposure to hemolysate but no other arachidonate was increased.
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PMID:[Effects of the subarachnoid hemorrhage on the release of arachidonate metabolites from canine cerebral arteries]. 354 66

The effect of subarachnoid hemorrhage (SAH) on endothelium-dependent vasodilation of isolated rabbit basilar artery was examined using an isometric tension recording method. Thirty-five rabbits that had 2 successive blood injections were divided into 3 groups: normal animals (control), 4 days, and 3 weeks after the first SAH. Acetylcholine (ACh) (10(-6)-10(-4) M) and adenosine triphosphate (ATP) (10(-6)-10(-4) M) were used to evoke dose-dependent vasodilation of isolated arterial rings previously contracted by 10(-6) M serotonin. In the animals killed 4 days after the first SAH, both ACh- and ATP-induced relaxation were suppressed, and the degree of relaxation of this group was 38 +/- 4.5% (mean +/- SEM) and 22 +/- 3.9% of the initial contractile tone in response to 10(-4) M ACh and 10(-4) M ATP, respectively. Suppression of the relaxation induced by ATP was seen even in the animals killed 3 weeks after the first SAH. Moreover, pretreatment with hemoglobin (10(-6) and 10(-5) M) inhibited endothelium-dependent vasodilation induced by ACh in the arterial rings from the animals killed 4 days after the first SAH. The present experiments suggest that impairment of the endothelium-dependent vasodilation following SAH may be involved in the pathogenesis of cerebral vasospasm.
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PMID:Impairment of endothelium-dependent vasodilation induced by acetylcholine and adenosine triphosphate following experimental subarachnoid hemorrhage. 356 7

Cerebral blood flow and cerebral metabolic rate for oxygen were measured during isoflurane-induced hypotension in 10 patients subjected to craniotomy for clipping of a cerebral aneurysm. Flow and metabolism were measured 5-13 days after the subarachnoid haemorrhage by a modification of the classical Kety-Schmidt technique using xenon-133 i.v. Anaesthesia was maintained with an inspired isoflurane concentration of 0.75% (plus 67% nitrous oxide in oxygen), during which CBF and CMRO2 were 34.3 +/- 2.1 ml/100 g min-1 and 2.32 +/- 0.16 ml/100 g min-1 at PaCO2 4.1 +/- 0.1 kPa (mean +/- SEM). Controlled hypotension to an average MAP of 50-55 mm Hg was induced by increasing the dose of isoflurane, and maintained at an inspired concentration of 2.2 +/- 0.2%. This resulted in a significant decrease in CMRO2 (to 1.73 +/- 0.16 ml/100 g min-1), while CBF was unchanged. After the clipping of the aneurysm the isoflurane concentration was reduced to 0.75%. There was a significant increase in CBF, although CMRO2 was unchanged, compared with pre-hypotensive values. These changes might offer protection to brain tissue during periods of induced hypotension.
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PMID:Cerebral blood flow and metabolism during isoflurane-induced hypotension in patients subjected to surgery for cerebral aneurysms. 367 49

A large unilateral subarachnoid hemorrhage (SAH) was created in 21 monkeys, and horseradish peroxidase (HRP) was injected into the cisterna magna or left internal carotid artery in 3 others (normals). Cerebral fixation was performed on Day 14 after SAH or 15 minutes after HRP injection. The major cerebral arteries from both the nonclot (control) and clot sides and the normal animals were examined with scanning and transmission electron microscopy (SEM and TEM). SEM of the adventitial surfaces of control and normal arteries revealed tunnel-like structures along the longitudinal axis. No vasa vasorum were seen, but adventitial rounded openings were observed, 10 to 35 micron in diameter in vessels of the anterior circulation and up to 80 micron in diameter in the basilar arteries. The stomas, numbering 5 to 10/mm of specimen, appeared to connect the subarachnoid and intraadventitial spaces or pathways. In SAH arteries, the tunica adventitia was coated with cellular remnants of hematoma or dense, well-organized blood clots, the removal of which revealed blocked stomas. TEM showed HRP in the vessel walls after injection into the cisterna magna, but not after injection into the carotid artery. TEM of control arteries revealed Virchow-Robin (intraadventitial) spaces lined by simple planar epithelium-like cells; Virchow-Robin spaces contained sparse nerve fiber bundles and connective tissue fibers. In SAH arteries, these spaces were almost filled with strands of connective tissue and fibroblasts; no nerve fibers were detected. Vasogenic substances probably reach smooth muscle cells via the adventitial stomas. SAH occluding the stomas may block the cerebrospinal fluid circulation, disturbing nutrition of the arterial wall or removal of wastes from it, thereby aggravating vasospasm.
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PMID:Electron microscopy of simian cerebral arteries after subarachnoid hemorrhage and after the injection of horseradish peroxidase. 380 41


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